The Chlamydia are obligate intracellular parasites of eukaryotic cells which are responsible for various diseases. They occupy an exclusive eubacterial phylogenic branch, having no close relationship to any other known organisms—they are classified in their own order (Chlamydiales) which contains a single family (Chlamydiaceae) which in turn contains a single genus (Chlamydia). Four species are currently known—C.trachomatis, C.pneumoniae, C.pecorum and C.psittaci. 
The Chlamydia undergo a developmental cycle in which two functionally and morphologically different cell types can be recognized: the extracellular elementary body (EB) and the intracellular reticulate body (RB). The developmental cycle is initiated by endocytosis of an EB by a eukaryotic host cell. The bacteria remain within an intracellular vacuole and, shortly after internalization, EBs reorganize and differentiate into RBs, which actively multiply. Late in the cycle, logarithmic growth ceases as RBs begin to restructure into EBs, which are released upon lysis of the host cell.
Chlamydia pneumoniae (also known as Chlamydophila pneumoniae and, previously, as TWAR) causes infections of the respiratory tract. It has been estimated [1] that it is responsible for up to 10% of all cases of community-acquired pneumonia and 5% of bronchitis and sinusitis cases. Studies have also suggested a role for C.pneumoniae in atherosclerosis and coronary heart disease [2].
The human serovariants (“serovars”) of C.trachomatis are divided into two biovariants (“biovars”). Serovars A-K elicit epithelial infections primarily in the ocular tissue (A-C) or urogenital tract (D-K). Serovars L1, L2 and L3 are the agents of invasive lymphogranuloma venereum. C.trachomatis is the leading cause of preventable infectious blindness (ocular trachoma) in the developing world and of sexually transmitted disease (“STD”) in the USA. Although antibiotic therapy can be effective, untreated or inadequately treated infections result in hundreds of thousands of cases of pelvic inflammatory disease each year in the USA.
Being intracellular, Chlamydia can generally evade antibody-mediated immune responses, and the importance of cell-mediated immune responses (CMI) during infections by obligate intracellular bacteria is being increasingly reported. In this context, induction of CD8+ cytotoxic T lymphocytes (CTLs) which are specific for peptides derived from the Major Outer Membrane protein (MOMP) of C.trachomatis has been described [3]. These CTLs are able to kill cervical epithelial cells infected by the pathogen, which suggests that immunisation with suitable CTL epitopes could represent a tool against this and closely related bacteria. Furthermore, activation of CMI responses is believed to be important for protective immunity against C.pneumoniae [4, 5, 6].
The identification of peptides derived from C.pneumoniae and C.trachomatis antigens which are able to bind to different classes of human class I MHC molecules will therefore be useful for the development of a CTL-based vaccine [e.g. references 7 & 8].
Genome sequences of C.pneumoniae [9, 10, 11, 12, 13] and C.trachomatis [12, 14, 15] are available. Although computer algorithms have been designed to predict T-cell epitopes from amino acid sequences [e.g. 16, 17, 18, 19], their predictions are not particularly accurate. For example, in a study carried out on human papillomavirus type 18 E6 antigen, only 8 out of 18 peptides identified by computer algorithms could actually bind to HLA-A0201 molecules [20].
It is an object of the invention to provide CTL epitopes from Chlamydia and to provide materials which can deliver these epitopes for immunisation.